TA-65 (cycloastragenol)
Mechanism, regulatory status, and an honest, tiered evidence map.
What it is
Class: Astragalus-derived telomerase activator (supplement)
Also known as: TA-65, cycloastragenol, TA-65MD
Relationship to telomere biology: TA-65 is a small-molecule telomerase activator, an improved formulation of cycloastragenol purified from Astragalus membranaceus. It is the most-studied human 'telomerase activator' supplement; its randomized human data measure telomere LENGTH (a contested biomarker), not any clinical or lifespan outcome.
Regulatory status
Sold as a dietary supplement by T.A. Sciences; not an approved drug and not approved for any anti-aging, longevity, or healthspan indication. Supplement status is a marketing pathway, NOT evidence of an aging benefit.
Mechanism
Reported to modestly activate telomerase (TERT) and, in a 1-year RCT, to increase measured telomere length in the low-dose arm. Telomere length is a contested biomarker and activating telomerase raises a cancer-risk question. See /telomerase-tert-terc, /telomere-length-biomarker, and /telomerase-cancer-paradox.
Animal lifespan evidence
Animal lifespan evidence: none in this dataset
No animal lifespan study for TA-65 is included in this dataset. The human evidence is telomere-length biomarker data only.
This is separate from human lifespan evidence, which is none for every intervention on this site. A mouse lifespan result is not a human lifespan result, and a telomere change is not a lifespan result in either species.
Evidence — Human (randomized, placebo-controlled — biomarker) verify: verified against primary source
| Species / population | 117 relatively healthy CMV-positive adults aged 53–87 (Salvador 2016); an earlier immune-focused study of older adults (Harley 2011). |
| Exposure, route, schedule | Oral TA-65 (low dose 250 U/day; high dose 1000 U/day) over 12 months in the RCT. |
| Comparator / duration | Placebo-controlled, double-blind, randomized; 1-year duration. |
| Endpoint / numeric result | Low-dose TA-65 increased median telomere length by ~530 bp over 12 months (p=0.005) while placebo lost ~290 bp (p=0.01); the high-dose arm showed a non-significant trend. Harley 2011 reported a decline in senescent (CD8+CD28−) T cells. |
| What it did NOT establish | Both endpoints are contested biomarkers (telomere length; immune-cell subsets), not clinical outcomes. No healthy-aging, disease-outcome, or lifespan benefit is established, and the data carry a commercial conflict of interest. |
Negative or null findings
- The high-dose (1000 U) arm did NOT significantly increase telomere length in Salvador 2016 — the significant effect was low-dose only, an unusual dose-response for a supplement.
- No clinical outcome, disease-outcome, or lifespan endpoint has been shown; the 2025 TA-65 meta-analysis (PMID 41286474) is confirmed, and its own conclusion is that telomere elongation did not translate into functional or inflammatory benefit.
The form used in the trials
A product-fact block, not a recommendation. It records the form the trials used and what they administered. TeloiX does not rank products, name a best one, suggest a dose, or claim an effect.
| Amount used in the trials | Oral TA-65 (low dose 250 U/day; high dose 1000 U/day) over 12 months in the RCT. |
| Trial population | 117 relatively healthy CMV-positive adults aged 53–87 (Salvador 2016); an earlier immune-focused study of older adults (Harley 2011). |
| Regulatory status | Sold as a dietary supplement by T.A. Sciences; not an approved drug and not approved for any anti-aging, longevity, or healthspan indication. Supplement status is a marketing pathway, NOT evidence of an aging benefit. |
Read the conflict-of-interest note above before you buy. The human data on this compound were authored by people with a commercial interest in it.
Find TA-65 (cycloastragenol) on Amazon →
The search returns several variants. The trials used TA-65, the branded T.A. Sciences formulation of cycloastragenol used in the Salvador 2016 randomized trial. See the conflict-of-interest note on this page.
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